PubMed · 14782849
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E RAJKA. 1950. [Physical allergy; physical allergodermatoses].. https://pubmed.ncbi.nlm.nih.gov/14782849/
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Contact dermatitis may be either irritant, allergic or both. The differential diagnosis is based on information from the patient, nature and concentration of chemicals involved and clinical examination. In case of suspicion of allergic contact dermatitis, the search for the responsible allergen(s) is built on patch testing. Positive patch test results, the current and/or past relevance of which has to be assessed, are confirmative. Additional tests, such as the repeated open application test, are sometimes recommended. Treatment which is symptomatic, is mainly based upon corticosteroids, either local or systemic; efficacy is rather limited. By any means, it cannot be substituted to the eviction of allergens. Primary and secondary prevention are linked with the complete eviction of allergens, but this caveat can be attenuated in some circumstances.
Oral ingestion or parenteral administration of certain contact allergens may elicit eczematous skin reactions "from inside" in sensitized individuals; this phenomenon has been termed "systemically-induced eczema" or "hematogenous contact eczema". There is a wide range of clinical features from polyetiological dyshidrotic hand and foot eczema to baboon syndrome. The most important contact allergens known to elicit systemically-induced contact eczema are metal salts, drugs, phytoallergens and balsam of Peru. Diagnosis is based on proof of delayed type hypersensitivity by patch testing and oral challenge. Until more and better data is acquired, special diets (for instance low nickel) should be instituted only in carefully selected patients.
In vitro and in vivo studies provide a body of evidence that adequate protection of the skin against ultraviolet (UV)-induced damage requires photostable broad-spectrum sunscreens with a proper level of UVA protection. UVA alone and UV solar simulated radiation (SSR) induce DNA lesions in keratinocytes and melanocytes as reflected by the comet assay and p53 accumulation. UVA and SSR impair the immune system as shown by significant alteration of Langerhans cells and inhibition of contact hypersensitivity response to chemical allergens and delayed-type hypersensitivity response to recall antigens. Any of these detrimental effects is more efficiently prevented by sunscreens with a higher level of protection in the UVA range. The involvement of UVA (fibroblast alteration, increased metalloproteinase expression) and the pivotal need for well-balanced UVA/UVB sunscreens were further demonstrated using reconstructed three-dimensional skin models.